Diacylglycerol acyltransferases : potential roles as pharmacological targets
Zammit, Victor A., Buckett, Linda K., Turnbull, Andrew V., Wure, Haja and Proven, Andrew. (2008) Diacylglycerol acyltransferases : potential roles as pharmacological targets. Pharmacology & Therapeutics, Vol.118 (No.3). pp. 295-302. ISSN 0163-7258Full text not available from this repository.
Official URL: http://dx.doi.org/10.1016/j.pharmthera.2008.03.010
Triglyceride (TG) synthesis occurs in many cell-types, but only the adipocyte is specialised for TG storage. The increased incidence of obesity and its attendant pathologies have increased interest in pharmacological strategies aimed at inhibition of triglyceride synthesis. In the liver this would also appear to offer the advantages of the prevention of steatosis and/or dyslipidaemia. The two major enzymes that have DGAT activity appear to have specialised functions, that are most evident in triglyceride-secreting tissues. The presence of triglyceride in non-adipose cells can lead to (through lipolysis), or be a marker for, undesirable complications such as insulin resistance, or can be indicative of simultaneously high capacities for triglyceride synthesis, lipolysis and oxidation of fatty acids as in highly aerobic, trained muscle. Consequently, inhibition of triglyceride synthesis may not be a straightforward strategy, either in terms of its achievement pharmacologically or in its anticipated outcomes. The metabolic complexities of triglyceride synthesis, with particular reference to the diacylglycerol acyltransferases (DGATs) are considered in this short review.
|Item Type:||Journal Article|
|Subjects:||R Medicine > R Medicine (General)|
|Divisions:||Faculty of Medicine > Warwick Medical School > Translational & Systems Medicine > Metabolic and Vascular Health
Faculty of Medicine > Warwick Medical School
|Journal or Publication Title:||Pharmacology & Therapeutics|
|Official Date:||June 2008|
|Page Range:||pp. 295-302|
|Access rights to Published version:||Restricted or Subscription Access|
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